Optokinetic nystagmus and parietal lobe lesions

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Abstract
In an attempt to define better the mechanism of impaired optokinetic nystagmus (OKN) caused by parietal lobe lesions, we recorded the eye movements of two patients. One had a slowly enlarging parietal glioma, and the other, an infarction involving the parietal and occipital lobes. In both patients, ipsilateral foveal pursuit and full‐field pursuit of a surrounding optokinetic drum were impaired while voluntary and involuntary saccades (fast components) were normal. Foveal pursuit was impaired more than full‐field pursuit, suggesting the existence of two separate pathways by which visual signals for OKN slow phases reach the oculomotor centers in the brainstem. We conclude that the ipsilateral slow phase OKN deficit seen in out patients resulted from damage to the foveal pursuit pathway that runs from the occipitoparietal association area to the ipsilateral brainstem horizontal gaze center.